Spontaneous intracerebral hemorrhage (ICH) is associated with greater mortality and more severe neurological deficits than any other stroke subtype. Initial mortality remains high at 26-50%, and survivors often have significant residual disability. To date, no medical or surgical therapy has been shown to improve outcome. Understanding the manner in which ICH induces brain injury is critical to developing effective treatments. Delayed neurological deterioration after ICH has been reported to occur in one-quarter to two-thirds of patients. While clinical worsening in association with hematoma enlargement is well-documented, few data are available delineating other causes of neurological deterioration following ICH in human subjects. This research plan will investigate the mechanism, extent and clinical importance of edema as a mechanism of secondary brain injury following ICH in human subjects using modern neuroimaging techniques. Two Specific Aims will be carried out. Specific Aim 1: To ascertain the time course, extent and clinical significance of brain edema formation in 20 patients with acute ICH.3D MPRAGE MRI and the brain boundary shift integral (BBSI) will be used to measure changes in brain volume in 20 patients with acute supratentorial ICH. Studies will be performed within 24 hours of ICH onset, on day 3-4, and on day 7 or discharge. Clinical course will be monitored on a daily basis during the first week. Twenty patients with ischemic stroke and twenty normal volunteers will serve as positive and negative controls, respectively. Specific Aim 2: To measure peri-clot blood brain barrier permeability in 20 patients with spontaneous supratentorial ICH. Initial measurements will be made with positron emission tomography (PET) and 11 C-methyl alpha aminoisobutyric acid (MeAIB) at 24-48 hours after onset and again on either day 3-4 (first 10 patients) or day 6-7 (second 10 patients). If Specific Aims 1 and 2 demonstrate that brain edema after acute ICH is associated with clinical deterioration, then trials of agents aimed at reducing brain edema, would be appropriate. We then would be able to use the BBSI and MelAB permeability to evaluate the physiological efficacy of different treatments and to choose appropriate agents and doses to design clinical intervention trials. If edema does not occur, it would suggest that design of such trials would be unlikely to improve patient outcome and other approaches to treatment should be sought.